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Coronary heart disease

Coronary heart disease (CHD), also called coronary artery disease (CAD) and atherosclerotic heart disease, is the end result of the accumulation of atheromatous plaques within the walls of the arteries that supply the myocardium (the muscle of the heart). While the symptoms and signs of coronary heart disease are noted in the advanced state of disease, most individuals with coronary heart disease show no evidence of disease for decades as the disease progresses before the first onset of symptoms, often a "sudden" heart attack, finally arise. After decades of progression, some of these atheromatous plaques may rupture and (along with the activation of the blood clotting system) start limiting blood flow to the heart muscle. more...

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Overview

Atherosclerotic heart disease can be thought of as a wide spectrum of disease of the heart. At one end of the spectrum is the asymptomatic individual with atheromatous streaks within the walls of the coronary arteries (the arteries of the heart). These streaks represent the early stage of atherosclerotic heart disease and do not obstruct the flow of blood. A coronary angiogram performed during this stage of disease may not show any evidence of coronary artery disease, because the lumen of the coronary artery has not decreased in caliber.

Over a period of many years, these streaks increase in thickness. While the atheromatous plaques initially expand into the walls of the arteries, eventually they will expand into the lumen of the vessel. As the plaques expand into the lumen of the vessel, they can affect the flow of blood through the arteries. While it was originally believed that the growth of atheromatous plaques was a slow, gradual process, some recent evidence suggests that the gradual buildup of plaque may be complemented by small plaque ruptures which cause the sudden increase in the plaque burden due to accumulation of thrombus material.

Atheromatous plaques that cause obstruction of less than 70 percent of the diameter of the vessel rarely cause symptoms of obstructive coronary artery disease. As the plaques grow in thickness and obstruct more than 70 percent of the diameter of the vessel, the individual develops symptoms of obstructive coronary artery disease. At this stage of the disease process, the patient can be said to have ischemic heart disease. The symptoms of ischemic heart disease are often first noted during times of increased workload of the heart. For instance, the first symptoms include exertional angina or decreased exercise tolerance.

As the degree of coronary artery disease progresses, there may be near-complete obstruction of the lumen of the coronary artery, severely restricting the flow of oxygen-carrying blood to the myocardium. Individuals with this degree of coronary heart disease typically have suffered from one or more myocardial infarctions (heart attacks), and may have signs and symptoms of chronic coronary ischemia, including symptoms of angina at rest and flash pulmonary edema.

A distinction should be made between myocardial ischemia and myocardial infarction. Ischemia means that the amount of oxygen supplied to the tissue is inadequate to supply the needs of the tissue. When the myocardium becomes ischemic, it does not function optimally. When large areas of the myocardium becomes ischemic, there can be impairment in the relaxation and contraction of the myocardium. If the blood flow to the tissue is improved, myocardial ischemia can be reversed. Infarction means that the tissue has undergone irreversible death due to lack of sufficient oxygen-rich blood.

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Antioxidant vitamins and coronary heart disease
From Nutrition Research Newsletter, 1/1/05

Epidemiologic studies have suggested that higher intakes of fruit, vegetables, and whole grain are related to a lower risk of coronary heart disease (CHD). One explanation for this finding is a reduction in oxidatively modified LDL, which is thought to play an important role in the development of atherosclerosis. Whether the association between these foods and CHD is due to antioxidant vitamins or some other factors remains unclear.

In the present Pooling Project of Cohort Studies on Diet and Coronary Disease, the authors studied the relations of the intakes of vitamin E, five carotenoids, and vitamin C to the incidence of all major CHD events and CHD mortality by pooling primary data from nine major cohorts studies. This large database enabled several issues to be examined, such as whether 1) single antioxidants or combinations of them predict CHD occurrence, 2) the strength of associations differs by dietary and supplemental intake and 3) non-dietary or dietary risk factors of CHD modify the association.

During a 10-year follow-up, 4,647 major incident CHD events occurred in 293,172 subjects who were free of CHD at baseline. Diet was measured by using a food frequency questionnaire in seven cohorts and by using a dietary history interview or food records in two cohorts. Overall intakes (dietary and supplemental combined) of vitamin E, beta-carotene, total carotene, and vitamin C were calculated.

There were significant inverse associations of intakes of energy-adjusted dietary vitamin E, alpha- and beta-carotene, lutein, and beta-cryptoxanthin with the incidence of all major CHD events in the pooled population not taking vitamin supplements. However, dietary intake of antioxidant vitamins was only weakly related to a reduced CHD risk after adjustment for potential non-dietary and dietary confounding factors. Subjects with higher supplemental vitamin C intake had a lower CHD incidence. Subjects in the highest quintile of vitamin C intake had a 24% lower risk than did those in the lowest quintile. Supplemental vitamin E intake was not significantly related to reduced CHD risk. A lower risk of major CHD events was found at higher total intakes of beta-carotene and at higher dietary intakes of several carotenoids after adjustment for age and energy intake.

The results of this study suggest that the use of vitamin C supplements may reduce CHD incidence in men and women. The findings weakly support the hypothesis that a higher dietary intake of vitamin E or lutein reduces the risk of CHD. However, further studies should be conducted regarding recommendations for high doses of vitamin C supplements.

Paul Knekt, John Ritz, Mark A Pereira, et al., Antioxidant vitamins and coronary heart disease rRisk: a pooled analysis of 9 cohorts, Am J Clin Nutr 80:1508--1520 (December 2004) [Address reprint requests to P Knekt, National Public Health Institute, Mannerheimintie 166, 00300 Helsinki, Finland. E-mail: paul.knekt@ktl.fi]

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